Effects of 5-HTTLPR genotype and cognitive rumination on long-term cortisol reactivity measured in human hair.

Ample experimental and associative studies have shown that carrying two short (S) alleles of the serotonin transporter gene (5-HTTLPR) contributes to an increased vulnerability for stress and related affective disorders. Recent findings indicate that this relationship might become even more profound when also possessing a negative ruminative (stress-related) thinking style. However, previous studies on the relationship among 5-HTTLPR, stress, and stress-responsiveness almost exclusively measured salivary cortisol concentrations during exposure to a single acute (laboratory) stressor. Measuring cortisol concentrations over longer periods of time might better reflect (chronic) Gene by biological (HPA) stress responsiveness associations. In recent years, the strategy to assess hair cortisol concentration (HCC) has been established as a more reliable marker for chronic HPA activations. The current study explored associations between 3-months accumulated HCC and the tendency to ruminate about negative events in 27 S/S and 27 L/L 5-HTTLPR-carriers (screened from a large n = 827 DNA database). Hierarchical regression (including moderation) analyses revealed clear significant interactions between Genotype and Rumination (p < 0.01, f2=0.26); indicating greatest accumulation of HCC in high ruminating S/S-allele carriers. These findings implicate that the combined possession of a genetic (S-allele 5-HTTLPR) and cognitive (Rumination) stress-vulnerability might meaningfully increases long-term stress responsiveness; most likely due to increased daily (chronic) stress experiences. Lay summary The current study investigated whether the combined possession of a biological (genetic) and cognitive (negative thinking pattern) stress vulnerability may lead to a greater vulnerability to experience daily stress. This hypothesis was confirmed as a higher accumulation of the cortisol stress hormone was found over the past 3 months in scalp hair of participants that carried both vulnerability factors in combination.

The interaction between 5-HTTLPR genotype and ruminative thinking on BMI.

Negative affect or stress is often found to increase energy intake for high palatable energy-rich foods and hence weight gain. Reduced brain serotonin (5-HT) function is known to increase stress vulnerability and the risk for eating-related disturbances. A short (S) allele polymorphism in the serotonin transporter gene (5-HTTLPR) is associated with a less efficient functioning brain serotonin system and therefore higher stress vulnerability. It has been suggested that this genotype may be directly linked to an increased risk for weight gain and/or obesity. However, a high amount of variability has been apparent in replicating such a direct gene on weight gain relationship. A most recent suggestion is that this gene by weight relationship might be moderated by an additional (cognitive) vulnerability factor involving repetitive negative thinking (rumination). Our objective was to investigate whether the S-allele of 5-HTTLPR contributes to weight gain particularly in high cognitive ruminating individuals. A total of 827 healthy young male and female college students (aged 21·3 (sd 3·0) years; BMI 16-41·7 kg/m2) were genotyped for the 5-HTTLPR polymorphism and assessed for rumination (Event Related Ruminative Index) and body weight. In line with the hypothesis, a hierarchical regression model showed that higher BMI scores were observed in specifically high ruminating S'-carriers (P=0·031, f²=0·022). These results suggest that cognitive rumination may be a critical moderator of the association between 5-HTTLPR and body mass.

Eating dependence and weight gain; no human evidence for a 'sugar-addiction' model of overweight.

BACKGROUND AND AIMS: There is an increasing societal concern that consumption of specific foods such as sugar might become 'addictive' and, hence, promote weight gain. Claims about the addictiveness of sugar however are based largely on findings from few animal studies, whereas there is a lack of direct human evidence for symptoms of sugar-related substance dependence. The current study examined in a large sample of human participants whether foods mainly containing sugar in particular might cause 'addiction-like' problems that meet clinical DSM criteria for substance dependence, and, also whether in turn this relates to body weight and negative affectivity (depressed mood). METHODS: In a cross-sectional study, n = 1495 university students from a variety of faculties were assessed for DSM-related signs of food addiction for particular food categories (YFAS), and, also BMI and negative affectivity. RESULTS: Results revealed that from the total sample, 95% experienced at least one symptom of food dependence and 12.6% met the YFAS classification for 'food addiction' as related to DSM-IV criteria. The majority of respondents experienced these problems for combined high-fat savoury (30%) and high-fat sweet (25%) foods, whereas only a minority experienced such problems for low-fat/savoury (2%) and mainly sugar-containing foods (5%). Overweight correlated only with addictive-like problems for high-fat savoury and high-fat sweet foods (P < 0.0001), while this was not found for foods mainly containing sugar. CONCLUSION: The current findings indicate that sugary foods contribute minimally to 'food dependence' and increased risk of weight gain. Instead, they are consistent with the current scientific notion that food energy density, and the unique individual experience of eating, plays an important role in determining the reward value of food and promoting excessive energy intake.

Gene by cognition interaction on stress-induced attention bias for food: Effects of 5-HTTLPR and ruminative thinking.

INTRODUCTION: Stress is often found to increase the preference and intake of high caloric foods. This effect is known as emotional eating and is influenced by cognitive as well as biological stress vulnerabilities. An S-allele of the 5-HTTLPR gene has been linked to decreased (brain) serotonin efficiency, leading to decreased stress resilience and increased risks for negative affect and eating related disturbances. Recently it has been proposed that a cognitive ruminative thinking style can further exacerbate the effect of this gene by prolonging the already increased stress response, thereby potentially increasing the risk of compensating by overeating high palatable foods. OBJECTIVE: This study was aimed at investigating whether there is an increased risk for emotional eating in high ruminative S/S-allele carriers reflected by an increased attention bias for high caloric foods during stress. METHODS: From a large (N=827) DNA database, participants (N=100) were selected based on genotype (S/S or L/L) and ruminative thinking style and performed an eye-tracking visual food-picture probe task before and after acute stress exposure. A significant Genotype x Rumination x Stress-interaction was found on attention bias for savory food; indicating that a stress-induced attention bias for specifically high-caloric foods is moderated by a gene x cognitive risk factor. CONCLUSION: Both a genetic (5-HTTLPR) and cognitive (ruminative thinking) stress vulnerability may mutually increase the risk for stress-related abnormal eating patterns.

Gene × cognition interaction on stress-induced eating: effect of rumination.

People often crave for high-caloric sweet foods when facing stress and this 'emotional eating' is a most important cause for weight gain and obesity. Eating under stress contrasts with the normally expected response of a loss of appetite, yet in spite of intensive research from neurobiological and cognitive disciplines we still do not know why stress or negative affect triggers overeating in so many of us. Since the prevalence of overweight and obesity still rises, the discovery of crucial risk factors is a most desirable goal of today's research on sub-optimal eating habits. This paper summarizes the most relevant current knowledge from the (human) literature regarding cognitive and biological vulnerabilities for stress-induced emotional eating. A (non-systematic) review of the most relevant studies reveals that most studies contemplate a rather one-directional way of focusing on either cognitive or biological factors, showing inconsistent results. The current paper elaborates and/or integrates these findings into a biological-cognitive interaction model in which a specific combination of genetic and cognitive vulnerabilities are thought to increase our bio-behavioral response to stress, critically increasing the rewarding value of pleasant foods and, hence, emotional eating.